University of Cambridge PhD Studentship in Cancer Biology 2026

Pancreatic ductal adenocarcinoma (PDAC) is a difficult type of pancreatic cancer to treat. One important recent development has been the creation of KRAS inhibitors, which are drugs that target KRAS, a protein that helps cancer cells grow. These drugs have shown promising results in clinical trials. For many years, KRAS was considered difficult to target with drugs. However, despite the progress made with KRAS inhibitors, cancer can quickly develop resistance to these treatments in both patients and laboratory mouse models. This creates an urgent need to understand why this resistance occurs and to find treatment combinations that can overcome it.

In our laboratory, we have developed and tested different PDAC models with varying genetic characteristics. Our studies have shown that the genetics of cancer cells can influence how they respond to treatment and can create different weaknesses that may be targeted with specific therapies. These effects can come from the cancer cells themselves as well as from changes in the cells and tissues surrounding the tumour. We therefore believe that interactions between cancer cells and surrounding cells, particularly in cancers with different genetic characteristics, may play an important role in resistance to KRAS inhibitors. Our research also shows that cancer-associated fibroblasts, which are cells found around tumours, can have different effects on pancreatic cancer and may activate pathways that help cancer cells resist treatment.

This PhD project will investigate how both the cancer cells themselves and the surrounding cells contribute to resistance to KRAS inhibitors in different types of PDAC. The research will focus particularly on PDAC genetic types for which we already have early evidence suggesting possible causes of drug resistance.

The project will use several complementary research methods, including growing cancer organoids and studying them in mouse models, using CRISPR to study the role of specific genes, single-cell RNA sequencing, flow cytometry, multiplex immunofluorescence, spatial transcriptomics, and other standard molecular biology techniques. A computational or bioinformatics component may also be available depending on the student's skills and interests. Together, these methods will help us understand how genetic differences within pancreatic tumours affect their response to KRAS inhibitors and how resistance develops.

Table of Content

• Summary
• Benefits
• Requirements
• Application Deadline
• How To Apply

Summary

• Application DeadlineOctober 16, 2026
• Study LevelPhD
• SponsorUniversity of Cambridge
• City to studyCambridge
• School to studyUniversity of Cambridge
• Course to studyBiology , Cancer Studies
• Eligible CountryAll Countries

Benefits

• Fully-funded PhD studentship (stated as fully-funded in the listing).
• Project combines in vivo models, organoids, in vivo CRISPR, single-cell RNA sequencing, flow cytometry, multiplex immunofluorescence, spatial transcriptomics, and molecular biology approaches.
• Computational component may be available depending on student skills and interests.

Requirements

We welcome applications from both UK and overseas students.

Application Deadline

How To Apply

Please apply via the University Applicant Portal at https://www.postgraduate.study.cam.ac.uk/courses/directory/cvcrpdmsc

You should select to commence study in October 2027.

Please quote reference SW51012 on your application and in any correspondence about this vacancy.

The University actively supports equality, diversity and inclusion and encourages applications from all sections of society.

The University has a responsibility to ensure that all employees are eligible to live and work in the UK.

For more information, visit University of Cambridge scholarship webpage.